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Summer 1998 Newsletter


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Organophosphate and Carbamate Insecticide Poisoning

 Organophosphate and carbamate insecticides are commonly used for small animals as flea and tick powders, sprays, foggers, shampoos and dips, flea collars, and formerly, as systemic insecticides. They are also frequently used as household, garden, and farm insecticides. Chlorpyrifos, parathion, diazinon, famphur, phorate, terbufos, and malathion are examples of organophosphates while carbofuran, aldicarb, and carbaryl, are carbamates. They are all marketed under a wide variety of trade names.

Both organophosphate and carbamates are highly toxic to all animals, including pets, livestock, and humans although some are far more toxic than others. All OP/Carbamate insecticides are fat soluble and therefore are easily absorbed through the skin and then transported throughout the body. These chemicals kill insects and cause poisoning in animals by inhibiting the enzyme, acetylcholinesterase (AChE) which normally functions to degrade acetylcholine in nerve synapses. Inhibition of AChE in the nerves results in a buildup of acetylcholine (ACh) and overstimulation of ACh receptors. Since all organophosphate and carbamate insecticides have the same mechanism of action and can be long-lasting, the effects of multiple exposures (for example: flea dip, flea powder, flea collar, and home and lawn flea treatment) are additive. There are two types of ACh receptors, muscarinic and nicotinic. Overstimulation of muscarinic receptors gives rise to the characteristic SLUDD signs of OP/Carbamate poisoning: salivation, lacrimation, urination, defecation, and dyspnea (due to increased bronchial secretions and bronchoconstriction), plus bradycardia and miosis. Overstimulation of nicotinic ACh receptors produces muscular fasiculations and tremors initially followed by flaccid paralysis. Death in acute poisonings is frequently due to respiratory failure resulting from inhibition of central (medullary) respiratory drive, excessive bronchial secretions, and bronchospasms coupled with depolarizing blockade at neuromuscular junctions (diaphragm and intercostals).

 The diagnosis of OP/Carbamate poisoning is made based on:

  1.  (1) History of exposure to one or more OP/Carbamates.
  1. Signs:
    1. Muscarinic signs: SLUDD + bradycardia and miosis.
    2. Nicotinic signs: muscle stiffness, muscle fasiculations, tremors, weakness, flaccid paralysis.
    3. CNS signs: restlessness, hyperactivity, seizures.
    4. Animals often found dead.

NOTE: Not all animals read the book and can present with any combination of the signs listed above.

  1. Blood ACh activity: usually less than 25% of normal with OP/Carbamate exposure. Whole blood must be submitted with an anticoagulant such as EDTA or heparin.
  1. Clinical Pathology: Some organophosphates have been associated with an increase in CPK and AST.
  1. Necropsy: There are no definitive gross or histological lesions in acute poisonings. Brain cholinesterase is significantly decreased. Stomach contents and liver are frequently used to diagnose OP/Carbamate poisoning and identify which chemical was responsible for the poisoning.

If OP/Caramate poisoning is suspected, the samples which should be taken and submitted for diagnosis are:

  1. Whole, unclotted blood, refrigerated as quickly as possible. Do not freeze.
  1. Frozen brain (one half of the brain frozen as quickly as possible.).
  1. Vomitus or stomach contents, frozen. This is often the best sample to positively identify which chemical is responsible for the poisoning.
  1. Liver, 25g, frozen.
  1. Eyeball for retinal cholinesterase activity. Remove and freeze as soon as possible. (Used primarily in large animal cases when no other samples are available.)
  1. Skin is not routinely tested, but can sometimes be used if exposure was dermal and no other samples are available.
  • NOTE: A full necropsy should always be performed and a full set of tissues submitted for histology to rule out other causes of death, particularly if legal action is a possibility.

 Organophosphate and carbamate poisoning is relatively common in pets and livestock. Animals can present with any combination of the muscarinic and/or nicotinic signs listed above or are frequently found dead. Diagnosis in live animals is based on a history of appropriate clinical signs, depressed blood acetylcholinesterase activity, and the identification of an OP/Carbamate in vomitus or stomach contents, if available. Diagnosis at necropsy is based on history, depressed brain or retinal acetylcholinesterase activity, and the identification of a specific OP/Carbamate in stomach contents and/or liver.

 - by Jennifer Harms, B.S.

Christina Wilson, B.S.

Robert Everson, PhD

Stephen Hooser, DVM, PhD


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